Although a sodium-dependent transporter for vitamin C exists, it is present mainly in specialized cells, whereas the glucose transporters, the most notable being GLUT1, transport Vitamin C (in its oxidized form, DHA)[3] in most cells, where recycling back to ascorbate generates the necessary enzyme cofactor and intracellular antioxidant, (see Transport to mitochondria).

The structure shown here for DHA is the commonly shown textbook structure. This 1,2,3-tricarbonyl is too electrophilic to survive more than a few milliseconds in aqueous solution, however. The actual structure shown by spectroscopic studies is the result of rapid hemiacetal formation between the 6-OH and the 3-carbonyl groups. Hydration of the 2-carbonyl is also observed.[4] The lifetime of the stabilized species is commonly said to be about 6 minutes under biological conditions.[1] Destruction results from irreversible hydrolysis of the ester bond, with additional degradation reactions following.[5] Crystallization of solutions of DHA gives a pentacyclic dimer structure of indefinite stability. Recycling of ascorbate via active transport of DHA into cells, followed by reduction and reuse, mitigates the inability of humans to synthesize it from glucose.[6]

Hydration equilibria of DHA - the hemiacetal structure (center) is the predominant one. (Water molecules are not actually involved in the first equilibrium, since it is an "internal" hemiacetalisation. Real hydration strictly occurs only in the middle carbonyl group)

Vitamin C does not pass from the bloodstream into the brain, although the brain is one of the organs that have the greatest concentration of vitamin C. Instead, DHA is transported through the blood–brain barrier via GLUT1 transporters, and then converted back to ascorbate.[7]

In a cell culturegrowth medium, dehydroascorbic acid has been used to assure the uptake of vitamin C into cell types that do not contain ascorbic acid transporters.[12]

As a pharmaceutical agent, some research has suggested that administration of dehydroascorbic acid may confer protection from neuronal injury following an ischemic stroke.[7] The literature contains many reports on the antiviral effects of vitamin C,[13] and one study suggests dehydroascorbic acid has stronger antiviral effects and a different mechanism of action than ascorbic acid.[14] Solutions in water containing ascorbic acid and copper ions and/or peroxide, resulting in rapid oxidation of ascorbic acid to dehydroascorbic acid, have been shown to possess powerful but short-lived antimicrobial, antifungal, and antiviral properties, and have been used to treat gingivitis, periodontal disease, and dental plaque.[15][16] A pharmaceutical product named Ascoxal is an example of such a solution used as a mouth rinse as an oral mucolytic and prophylactic agent against gingivitis.[16][17] Ascoxal solution has also been tested with positive results as a treatment for recurrent mucocutaneous herpes,[17] and as a mucolytic agent in acute and chronic pulmonary disease such as emphysema, bronchitis, and asthma by aerosol inhalation.[18]